| Size | Price | Stock | Qty |
|---|---|---|---|
| 1mg |
|
||
| 5mg |
|
||
| 10mg |
|
||
| 25mg |
|
||
| 50mg |
|
||
| 100mg |
|
||
| Other Sizes |
| Targets |
Ras and RAF
MCP110 specifically targets the protein-protein interaction between the small GTPase Ras (including its oncogenic mutant H-Ras (V12)) and its downstream effector, the serine/threonine-protein kinase Raf-1 (c-Raf). By acting as an inhibitor of this interaction, MCP110 prevents the formation of the Ras-Raf-1 complex, which is a crucial step in the activation of the mitogen-activated protein kinase (MAPK) signaling cascade. This disruption is key to its mechanism, as aberrant signaling through this pathway is a hallmark of many human tumors. |
|---|---|
| ln Vitro |
In HEK293 cells, MCP110 (10 and 20 μM) suppresses the activation of AP-1 triggered by H-Ras (V12). The activation of Raf-1 activity by Ras is greatly reduced when MCP110 (20 μM) is present [1]. In fibrosarcoma HT1080 cells, MCP110 (1, 2, 5, 10 and 20 μM) shows dose-dependent suppression of increased Raf-1 activity [1]. Growth factors caused by serum, phorbol 12-myristate 13-acetate (100 nM), platelet-derived growth factor in A549 cells (20 ng/mL), and EGF (100 ng/mL) are all reduced by MCP110 (20 μM)[1].
In vitro, MCP110 demonstrates potent inhibitory activity in several cellular models. In HEK293 cells, treatment with MCP110 at 10 and 20 μM suppresses the activation of AP-1 (activator protein-1) that is triggered by the oncogenic H-Ras (V12) mutant. Furthermore, in fibrosarcoma HT1080 cells, MCP110 exhibits a dose-dependent suppression of elevated Raf-1 activity at concentrations of 1, 2, 5, 10, and 20 μM. The presence of 20 μM MCP110 significantly reduces the ability of Ras to stimulate Raf-1 activity. It also decreases the level of cyclin D stimulated by various growth factors such as EGF, PDGF, and serum in A549 cells. |
| ln Vivo |
In vivo studies for MCP110 are primarily based on its potential as a research tool for tumor biology. By disrupting the Ras/Raf-1 interaction, it is hypothesized to revert Ras-dependent transformation phenotypes in human cancer cells, as suggested by its in vitro mechanism. This makes it a valuable compound for investigating the effects of inhibiting this specific protein-protein interaction in animal models of cancer. However, specific published in vivo efficacy data for MCP110 in animal models are not extensively detailed in standard literature, as it remains a research-grade compound primarily used for target validation.
|
| Enzyme Assay |
In vitro enzyme/receptor binding studies for MCP110 are focused on its ability to disrupt the Ras/Raf-1 interaction. These are typically conducted using cell-based assays rather than isolated enzyme systems. For example, the disruption is measured indirectly by assessing the decrease in downstream signaling events such as Raf-1 activity or AP-1 activation in cells expressing oncogenic Ras. While the assay is cell-based, the readout is the inhibition of a specific protein-protein interaction and subsequent signaling pathway, which is a hallmark of a non-cellular, biochemical interaction being evaluated in a cellular context.
|
| Cell Assay |
In vitro cellular assays are the primary method for characterizing MCP110's activity. In these experiments, cancer cell lines, such as HT1080 fibrosarcoma cells or A549 lung carcinoma cells, are treated with varying concentrations of MCP110 (ranging from 1 to 20 μM). The effects are then measured by assessing the activity of downstream signaling molecules. Key readouts include Raf-1 kinase activity, AP-1 reporter activity, and the expression of target genes like cyclin D. These assays help to confirm the compound's mechanism of action and potency in a living cellular environment.
|
| Animal Protocol |
In vivo animal studies for MCP110 are not extensively documented in the provided search results. However, based on its mechanism as a Ras/Raf-1 interaction inhibitor, it is a prime candidate for study in xenograft models. In such models, tumor-bearing mice would be treated with MCP110 to assess its effect on tumor growth, which would be correlated with the inhibition of the MAPK pathway in the tumor tissue. While specific protocols are not detailed, these studies would typically involve administering the compound (likely via intraperitoneal injection) and monitoring tumor volume, survival, and pharmacodynamic markers.
|
| ADME/Pharmacokinetics |
Pharmacokinetic properties of MCP110 are not comprehensively detailed in the available sources. However, key physicochemical properties are known. It has a molecular weight of 508.66 g/mol and a molecular formula of C₃₃H₃₆N₂O₃. The compound is soluble in DMSO at 250 mg/mL, which is relevant for preparing stock solutions for in vitro and in vivo studies. Its LogP value is 6.24, indicating high lipophilicity, which may influence its absorption and distribution. For storage, it is recommended to store the powder at -20°C for up to 3 years.
|
| Toxicity/Toxicokinetics |
Toxicological data for MCP110 are limited as it is a research compound not intended for human use. It is primarily used in laboratory settings, and standard safety precautions should be followed when handling it. While specific toxicity profiles are not detailed, its mechanism of inhibiting the Ras/Raf-1 interaction could potentially affect normal cell signaling pathways, leading to off-target effects. However, comprehensive toxicological studies are not available in the public domain, as its use is confined to preclinical research.
|
| References | |
| Additional Infomation |
MCP110 is a research-use-only chemical compound that functions as an inhibitor of the Ras/Raf-1 interaction. It was identified through two-hybrid screening as a compound that can revert Ras-dependent transformation phenotypes. This compound is part of a class of molecules aimed at disrupting protein-protein interactions that are critical for oncogenic signaling. It is not an approved drug and has no established clinical applications. Its primary value is as a tool for researchers to study the biological consequences of disrupting the Ras-Raf-1 axis in cancer models.
|
| Molecular Formula |
C33H36N2O3
|
|---|---|
| Molecular Weight |
508.66
|
| Exact Mass |
508.272
|
| CAS # |
521310-51-0
|
| PubChem CID |
10229237
|
| Appearance |
Colorless to light yellow ointment
|
| Density |
1.1±0.1 g/cm3
|
| Boiling Point |
686.3±55.0 °C at 760 mmHg
|
| Flash Point |
368.8±31.5 °C
|
| Vapour Pressure |
0.0±2.1 mmHg at 25°C
|
| Index of Refraction |
1.594
|
| LogP |
6.24
|
| Hydrogen Bond Donor Count |
0
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
14
|
| Heavy Atom Count |
38
|
| Complexity |
646
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
COC1=C(C=CC(=C1)CN(CCC2=CC=CC=N2)C(=O)CCCCC3=CC=CC=C3)OCC4=CC=CC=C4
|
| InChi Key |
JWLZIHLAMJDONF-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C33H36N2O3/c1-37-32-24-29(19-20-31(32)38-26-28-15-6-3-7-16-28)25-35(23-21-30-17-10-11-22-34-30)33(36)18-9-8-14-27-12-4-2-5-13-27/h2-7,10-13,15-17,19-20,22,24H,8-9,14,18,21,23,25-26H2,1H3
|
| Chemical Name |
N-[(3-methoxy-4-phenylmethoxyphenyl)methyl]-5-phenyl-N-(2-pyridin-2-ylethyl)pentanamide
|
| Synonyms |
MCP 110 MCP-110 MCP110
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO : ~250 mg/mL (~491.50 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.09 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (4.09 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.9659 mL | 9.8297 mL | 19.6595 mL | |
| 5 mM | 0.3932 mL | 1.9659 mL | 3.9319 mL | |
| 10 mM | 0.1966 mL | 0.9830 mL | 1.9659 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
